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📋 PRIMARY OPEN-ANGLE GLAUCOMA (POAG)

MS Ophthalmology Examination Notes — Based on Kanski's 10th Edition

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SECTION 1: DEFINITION

POAG = Chronic, progressive optic neuropathy of adult onset characterized by:

• Retinal nerve fibre layer (RNFL) thinning
• Glaucomatous optic nerve damage
• Characteristic visual field loss
• Open anterior chamber angle
• Absence of secondary glaucoma signs
• IOP is a key modifiable risk factor

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SECTION 2: PATHOGENESIS — FLOWCHART

TRIGGER: Elevated IOP / Vascular insufficiency / Genetic predisposition
                            │
                            ▼
        ┌─────────────────────────────────────┐
        │   MECHANICAL THEORY                 │
        │   IOP compresses axons at           │
        │   lamina cribrosa                   │
        │   → Axoplasmic flow disruption      │
        └──────────────┬──────────────────────┘
                       │         +
        ┌──────────────▼──────────────────────┐
        │   VASCULAR / ISCHAEMIC THEORY        │
        │   IOP compresses blood vessels       │
        │   → Optic nerve head ischaemia       │
        │   → Low ocular perfusion pressure    │
        └──────────────┬──────────────────────┘
                       │
                       ▼
         RETINAL GANGLION CELL (RGC) INJURY
                       │
                       ▼
         Ca²⁺ influx into RGC cell body
         + ↑ intracellular nitric oxide
         + Glutamine metabolism disruption
                       │
                       ▼
         RGC DEATH via APOPTOSIS
         (Programmed cell death — NOT necrosis)
                       │
                       ▼
         Astrocyte + glial cell proliferation
         + Extracellular matrix changes at lamina cribrosa
                       │
                       ▼
         OPTIC NERVE HEAD REMODELLING
                       │
                       ▼
         RNFL THINNING → OPTIC CUP ENLARGEMENT
         → VISUAL FIELD LOSS

Key point for exam: RGC death = APOPTOSIS. Pre-terminal event = Ca²⁺ influx + ↑ nitric oxide.

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SECTION 3: GENETICS — FLOWCHART

POAG GENETICS
       │
       ├─── 127+ loci identified in human genome (Nature Communications, 2021)
       │
       ├─── KEY GENES:
       │       │
       │       ├── MYOC gene → codes for MYOCILIN protein
       │       │   (found in trabecular meshwork)
       │       │   • Various mutations described
       │       │   • Normal function still undetermined
       │       │   • If glaucoma onset <35 yrs in a family member
       │       │     → chance of MYOC mutation UP TO 33%
       │       │
       │       └── OPTN gene → codes for OPTINEURIN
       │           • Broadly accepted as causing glaucoma
       │
       ├─── INHERITANCE PATTERN:
       │       • Siblings: 4× risk
       │       • Offspring: 2× risk
       │       • Genetic investigation if ≥3 first-degree relatives
       │         from 2 generations affected
       │
       └─── POLYGENIC RISK SCORE (PRS):
               • Predicts glaucoma susceptibility
               • Predicts risk of advanced disease
               • Future: personalised treatment thresholds

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SECTION 4: RISK FACTORS

4A. POSITIVE RISK FACTORS (Increase risk)

4B. NEGATIVE / PROTECTIVE FACTORS (Reduce risk or not proven)

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4C. HISTORY TAKING — WHAT TO ASK

HISTORY IN POAG
│
├── SYMPTOMS (usually NONE until advanced)
│   └── Peripheral field loss → tubular vision → central loss (late)
│       Occasionally: symptomatic central field defects early in NTG
│
├── OPHTHALMIC HISTORY
│   ├── Refractive error (myopia → POAG risk; hypermetropia → PACG risk)
│   ├── Previous trauma / inflammation
│   └── Prior eye surgery (affects IOP reading)
│
├── FAMILY HISTORY
│   ├── POAG / Ocular hypertension (OHT)
│   └── Other ocular disease
│
├── PAST MEDICAL HISTORY
│   ├── Asthma / heart failure / heart block / peripheral vascular disease
│   │   (contraindications to beta-blockers)
│   ├── Head injury / stroke / intracranial pathology
│   │   (may mimic VF loss)
│   ├── Vasospasm — migraine / Raynaud phenomenon
│   ├── Diabetes, systemic hypertension, cardiovascular disease
│   └── Oral contraceptive use
│
├── CURRENT MEDICATIONS
│   ├── Steroids (topical skin / inhaled / systemic)
│   ├── Oral beta-blockers (lower IOP)
│   └── Anti-VEGF injections
│
├── SOCIAL HISTORY
│   └── Smoking, alcohol (rule out toxic/nutritional optic neuropathy)
│
└── ALLERGIES
    └── Sulfonamide allergy → acetazolamide CONTRAINDICATED

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SECTION 5: EXAMINATION FINDINGS

5A. SLIT LAMP EXAMINATION

SLIT LAMP — WHAT TO LOOK FOR IN POAG SUSPECT
│
├── ANTERIOR SEGMENT
│   ├── Cornea: rule out pigment (Krukenberg spindle → pigment dispersion)
│   ├── Anterior chamber: depth (shallow → angle closure risk)
│   ├── Iris: transillumination defects (pigment dispersion)
│   │         pseudoexfoliation deposits at pupil margin
│   └── Lens: pseudoexfoliation material on anterior surface
│
├── PUPILS
│   ├── Check for RAPD (relative afferent pupillary defect)
│   └── If RAPD develops later → indicator of substantial progression
│
├── COLOUR VISION
│   └── Ishihara — if colour loss suggests NON-glaucomatous optic neuropathy
│
└── KEY: Exclude SECONDARY glaucoma causes (pigmentary, pseudoexfoliation)

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5B. TONOMETRY

IOP MEASUREMENT
│
├── GOLDMANN APPLANATION TONOMETRY (GAT) — Gold Standard
│   ├── Applied to corneal apex
│   ├── Measures force to flatten 3.06mm diameter area
│   └── Normal IOP: 10–21 mmHg (population mean ~15.5 mmHg)
│
├── PACHYMETRY (CCT) — always do before tonometry interpretation
│   ├── Thin CCT (<555μm) → underestimates IOP → higher true risk
│   ├── Thick CCT (>590μm) → overestimates IOP → lower true risk
│   └── Note time of day — diurnal variation up to 5 mmHg
│
├── NON-CONTACT TONOMETRY (air puff) — screening use
│
├── iCARE REBOUND TONOMETRY — no anaesthesia needed
│
└── ASYMMETRY: ≥4 mmHg difference between eyes is significant

PROGRESSION RISK FACTORS FROM EMGT:
(a) Magnitude of initial IOP reduction
(b) Height of baseline IOP
(c) Pseudoexfoliation syndrome
(d) Bilateral disease
(e) Worse mean deviation
(f) Older age

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5C. GONIOSCOPY

GONIOSCOPY IN POAG
│
├── PURPOSE: Confirm OPEN angle (rule out angle closure or secondary causes)
│
├── WHAT YOU SEE (Shaffer grading, nasal to cornea):
│   ├── Schwalbe line (SL) — anterior limit
│   ├── Trabecular meshwork (TM) — pigmented band
│   ├── Scleral spur (SS) — white band
│   ├── Ciliary body band (CBB) — grey/brown
│   └── Iris root
│
├── IN POAG:
│   ├── Angle WIDE OPEN — all structures visible
│   ├── TM may show variable pigmentation
│   └── No peripheral anterior synechiae (PAS)
│
├── LENS OPTIONS:
│   ├── Goldmann 3-mirror (indirect — image inverted)
│   └── Zeiss/Sussman 4-mirror (direct — no mirror inversion)
│
└── KEY EXAM POINT:
    • POAG = open angle
    • Gonioscopy is MANDATORY before diagnosing ANY glaucoma
    • Angle must be open in ALL quadrants

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5D. FUNDUS EXAMINATION — OPTIC DISC CHANGES

Normal Optic Disc (Know Before Abnormal)

NORMAL DISC
│
├── Neuroretinal rim (NRR): orange-pink tissue between cup and disc margin
├── ISNT Rule: Inferior > Superior > Nasal > Temporal rim width (broadest to narrowest)
├── Cup/disc (C/D) ratio: vertical C/D ratio used
│   ├── Only 2% population has C/D >0.7
│   └── Asymmetry ≥0.2 between eyes = suspicious
├── Normal disc vertical diameter: 1.5–1.7 mm (white population)
└── Small disc = small cup (may be normal); Large disc = large cup (may be normal)

Glaucomatous Optic Disc Changes — FLOWCHART

EARLY CHANGES
│
├── Increased C/D ratio (vertical > horizontal)
├── Focal NRR notching (especially inferior pole — inferotemporal is FIRST affected)
├── ISNT rule VIOLATED
├── Asymmetry of C/D ≥0.2 between eyes
├── RNFL defects (slit/wedge-shaped, superior or inferior arcuate zones)
└── Disc haemorrhage (splinter — infero-temporal, risk factor for progression)
              │
              ▼
PROGRESSIVE CHANGES
│
├── Generalised enlargement of cup (concentric)
├── Bayonetting sign — vessels disappear over rim edge, reappear in cup
├── Vertical elongation of cup
├── NRR becoming thinner
├── Vessel nasalisation (vessels displaced to nasal side)
└── Baring of circumlinear vessels
              │
              ▼
ADVANCED / LATE CHANGES
│
├── Bean-pot cupping (overhanging edges)
├── Cup-disc ratio approaching 1.0
├── Near total NRR loss
├── Pallor of remaining rim
├── Peripapillary atrophy (beta-zone most significant)
└── Disc haemorrhages (more common in NTG)

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5E. PERIMETRY (Visual Fields)

STANDARD AUTOMATED PERIMETRY (SAP) — Humphrey Field Analyser
│
├── Relatively INSENSITIVE in early disease
├── 25–35% of RGC lost before field defect detected
│
├── EARLY DEFECTS:
│   ├── Increased response variability (before actual defects)
│   ├── Paracentral scotoma — superonasal (most common first defect)
│   ├── Nasal step — sensitivity difference above/below horizontal midline
│   └── Temporal wedge
│
├── PROGRESSIVE DEFECTS:
│   ├── Arcuate (Bjerrum) scotoma — follows RNFL arc above/below fixation
│   ├── Seidel scotoma — comet-shaped extension from blind spot
│   ├── Ring scotoma (double arcuate)
│   └── Central field loss
│
├── ADVANCED DEFECTS:
│   ├── Altitudinal defect
│   └── Tubular/gun-barrel vision (central island + temporal island remaining)
│
├── SPECIAL MODALITIES:
│   ├── FDT (Frequency Doubling Technology) — detects defects EARLIER
│   ├── SWAP (Short Wavelength Automated Perimetry) — earlier defects
│   └── SITA (Swedish Interactive Threshold Algorithm) — fast, standard strategy
│
├── GLOBAL INDICES:
│   ├── Mean Deviation (MD) — average sensitivity loss
│   ├── Pattern Standard Deviation (PSD) — localized loss
│   └── Visual Field Index (VFI) — percentage of normal function
│
└── PROGRESSION: Change in MD >1 dB/year = clinically significant progression
    EMGT natural history (untreated):
    • HTG: -1.31 dB/year
    • NTG: -0.36 dB/year
    • PXEG: -3.13 dB/year

---

5F. OCT (Optical Coherence Tomography)

OCT IN GLAUCOMA — Has largely superseded other imaging
│
├── WHAT IT MEASURES:
│   ├── RNFL thickness (peripapillary — 3.46mm circle around disc)
│   ├── Optic disc parameters (rim area, C/D ratio)
│   ├── Ganglion cell complex (GCC) / macular GCL thickness
│   └── Bruch's membrane opening — minimum rim width (BMO-MRW)
│
├── TSNIT GRAPH (Temporal-Superior-Nasal-Inferior-Temporal):
│   ├── Normal: "double hump" pattern (superior and inferior peaks)
│   ├── Glaucoma: loss of inferior hump FIRST (inferotemporal RNFL)
│   └── Colour code: GREEN = normal, YELLOW = borderline, RED = abnormal
│
├── EARLY GLAUCOMA FINDINGS:
│   ├── Inferotemporal RNFL thinning (first area affected)
│   ├── Superior RNFL thinning (second)
│   ├── Ganglion cell layer thinning inferior to fovea
│   └── Macular GCL thinning — may detect earlier than perimetry
│
├── PROGRESSION MONITORING:
│   ├── Serial RNFL maps compared over time
│   ├── Trend-based analysis (slope of change)
│   └── Guided progression analysis (GPA)
│
└── IMPORTANT: OCT detects structural changes BEFORE visual field defects
    → "Structure before function" principle

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SECTION 6: TREATMENT PROTOCOL

6A. TREATMENT GOAL

PRIMARY AIM: Prevent functional vision impairment within patient's lifetime
             by REDUCING IOP (only proven method)

TARGET PRESSURE:
├── Based on: severity of damage (C/D ratio, MD on VF), pre-treatment IOP,
│            CCT, rate of progression, age, general health
├── Reasonable initial goal: IOP < 18 mmHg
│   (AGIS trial: visual field progression unlikely if IOP <18 mmHg at ALL times)
└── If target not achieved → adjust target lower
    If progression despite target → consider surgery

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6B. MEDICAL THERAPY — STEP-BY-STEP

STEP 1 — FIRST LINE: PROSTAGLANDIN ANALOGUES (PGAs)
│
├── Mechanism: ↑ uveoscleral outflow (mainly); some ↑ trabecular outflow
├── IOP reduction: 27–35% from baseline
├── Dosing: ONCE daily (bedtime)
├── Systemic side effects: MINIMAL
│
├── AGENTS:
│   ├── Latanoprost 0.005% — fewest ocular adverse events; used first
│   ├── Travoprost 0.004% — fewer non-responders; Polyquad preservative
│   ├── Bimatoprost 0.03% — greatest IOP reduction; more hyperaemia
│   │   (0.01% — same IOP reduction, less hyperaemia)
│   ├── Tafluprost — preservative-free; good for ocular surface disease
│   └── Omidenepag 0.002% — new EP2 agonist; no periorbitopathy; 5% hyperaemia
│
├── KEY SIDE EFFECTS:
│   ├── Conjunctival hyperaemia (most common)
│   ├── Increased iris pigmentation (irreversible)
│   ├── Eyelash growth (hypertrichosis)
│   ├── Periorbital fat atrophy (periorbitopathy — deepened upper lid sulcus)
│   └── CMO (cystoid macular oedema) — in aphakic/pseudophakic eyes
│
└── NOTE: Never use 2 PGAs together → paradoxical IOP RISE

              │ If IOP inadequate
              ▼

STEP 2 — ADD: BETA-BLOCKER
│
├── Timolol 0.25% or 0.5% — twice daily (or gel-forming — once daily)
├── Betaxolol — cardioselective (safer in mild asthma)
├── Mechanism: ↓ aqueous humour production
├── IOP reduction: 20–25%
│
└── CONTRAINDICATIONS:
    ├── Asthma / COPD
    ├── Heart failure
    ├── Heart block (2nd/3rd degree)
    └── Peripheral vascular disease

              │ If IOP still inadequate
              ▼

STEP 3 — ADD: CARBONIC ANHYDRASE INHIBITOR (CAI)
│
├── TOPICAL: Dorzolamide 2% (TDS) / Brinzolamide 1% (BD-TDS)
├── SYSTEMIC: Acetazolamide 250–500 mg (short-term only)
│   (Contraindicated if sulfonamide allergy)
├── Mechanism: ↓ aqueous production by inhibiting CA-II in ciliary epithelium
└── IOP reduction: 15–20%

              │ If IOP still inadequate
              ▼

STEP 4 — ADD: ALPHA-2 AGONIST
│
├── Brimonidine 0.15–0.2% (BD-TDS)
├── Mechanism: ↓ aqueous production + ↑ uveoscleral outflow
├── IOP reduction: 20–25%
├── Additional: possible neuroprotective effect
└── SIDE EFFECTS: allergy/follicular conjunctivitis (15%), fatigue, dry mouth
    AVOID in children <2 yrs (CNS depression)

              │ If IOP still inadequate
              ▼

STEP 5 — FIXED COMBINATIONS (improve adherence)
│
├── Timolol + Dorzolamide (Cosopt)
├── Timolol + Brimonidine (Combigan)
├── Timolol + Latanoprost (Xalacom)
└── Timolol + Bimatoprost (Ganfort)

              │ If max medical therapy fails
              ▼

STEP 6 — LASER / SURGICAL THERAPY

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6C. LASER TREATMENT

SELECTIVE LASER TRABECULOPLASTY (SLT)
│
├── Laser: Q-switched Nd:YAG, 532 nm
├── Target: Pigmented TM cells selectively
├── Energy: 0.4–1.2 mJ; 50 spots over 180° or 360°
├── IOP reduction: 20–30%
├── Repeatable (unlike ALT)
├── Can be used as FIRST LINE (LiGHT trial: SLT = first-line drops at 3 yrs)
└── Side effects: transient IOP spike, mild iritis

ARGON LASER TRABECULOPLASTY (ALT) — older, largely replaced by SLT
├── Burns TM, causing mechanical stretching
└── Not easily repeatable (scarring)

LASER IRIDOTOMY — for angle closure, NOT POAG (but know it)

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6D. SURGICAL TREATMENT

TRABECULECTOMY — Gold standard filtering surgery
│
├── Creates new aqueous drainage pathway (fistula) under conjunctival bleb
├── Anti-metabolites:
│   ├── Mitomycin C (MMC) — more potent, longer effect
│   └── 5-Fluorouracil (5-FU) — less potent, multiple injections
├── Target IOP: <15 mmHg achievable
├── Complications:
│   ├── Bleb failure (fibrosis)
│   ├── Hypotony (over-drainage)
│   ├── Bleb-related infection (blebitis → endophthalmitis)
│   └── Cataract progression

GLAUCOMA DRAINAGE DEVICES (GDD) — Tube surgery
├── Ahmed, Baerveldt, Molteno implants
├── Used when trabeculectomy failed or high risk
└── IOP reduction reliable, moderate

NON-PENETRATING FILTERING SURGERY
├── Deep sclerectomy — Descemet window created; collagen implant + goniopuncture
└── Viscocanalostomy — Schlemm canal dilated with viscoelastic

MINIMALLY INVASIVE GLAUCOMA SURGERY (MIGS) — Most Recent
│
├── GROUP 1 — Schlemm canal procedures (NO bleb):
│   ├── Trabectome — electro-ablation of TM (ab interno)
│   ├── Kahook Dual Blade — excise TM strip
│   ├── iStent inject — 2 titanium stents bypassing TM
│   └── Hydrus Microstent — scaffold to dilate Schlemm canal
│
├── GROUP 2 — Subconjunctival drainage (BLEB-forming):
│   ├── Xen Gel Stent — 45-micron lumen gelatin tube
│   ├── Preserflo MicroShunt — SIBS polymer
│   └── (± MMC injection at time of insertion)
│
└── GROUP 3 — Supraciliary/suprachoroidal drainage (NO bleb):
    └── MINIject — silicone implant into supraciliary space

INDICATIONS FOR MIGS:
├── Mild to moderate glaucoma
├── Target IOP: 15–17 mmHg
└── Often combined with phacoemulsification (cataract + glaucoma together)

CYCLODIODE LASER (CYCLOABLATION)
├── Destroys ciliary body epithelium → ↓ aqueous production
└── Reserved for end-stage / pain relief

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6E. TREATMENT ALGORITHM — SUMMARY FLOWCHART

NEWLY DIAGNOSED POAG
         │
         ▼
CONFIRM DIAGNOSIS (IOP, gonioscopy, disc, VF, OCT)
         │
         ▼
SET TARGET IOP (based on damage severity, CCT, age)
         │
         ▼
START: PROSTAGLANDIN ANALOGUE (once daily bedtime)
         │
    IOP at target? ──YES──→ MONITOR (every 3–6 months)
         │NO
         ▼
ADD: BETA-BLOCKER (or CAI if contraindicated)
         │
    IOP at target? ──YES──→ MONITOR
         │NO
         ▼
ADD: 3rd AGENT or FIXED COMBINATION
         │
    IOP at target? ──YES──→ MONITOR
         │NO
         ▼
CONSIDER: SLT LASER (can also use as 1st line — LiGHT trial)
         │
    IOP at target? ──YES──→ MONITOR
         │NO
         ▼
SURGICAL OPTIONS:
├── Mild-Moderate → MIGS (especially if combined with cataract surgery)
├── Moderate-Severe → TRABECULECTOMY ± MMC
└── Failed trabeculectomy / High risk → TUBE (GDD)
         │
    Still progressing despite target IOP?
         │
         ▼
LOWER TARGET FURTHER + Consider cyclodiode (end-stage)

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SECTION 7: MONITORING PROTOCOL

MONITORING IN POAG
│
├── FREQUENCY:
│   ├── Newly diagnosed / medication change: 4–6 weeks (IOP check)
│   ├── Stable, controlled: every 3–6 months
│   └── Visual fields: at least annually (more often if progressing)
│
├── EACH VISIT:
│   ├── VA, IOP (note time of day)
│   ├── Slit lamp (disc appearance, bleb if post-op)
│   ├── VF (annual or biannual)
│   └── OCT RNFL (annual or biannual)
│
└── PROGRESSION CRITERIA:
    ├── VF: MD change >1 dB/year, confirmed on ≥2 tests
    ├── OCT: Significant RNFL thinning on serial measurements
    └── Disc: New haemorrhage, notch enlargement, NRR loss

---

SECTION 8: SCREENING

WHO TO SCREEN (High-risk case finding):
│
├── Age >40 yrs with 1st-degree family history of POAG
├── All individuals >60 yrs (especially African descent from age 40)
├── African / Afro-Caribbean racial background
└── Myopes, OHT patients

SCREENING COMPONENTS (tonometry alone is INSUFFICIENT):
├── Tonometry (IOP)
├── Visual field assessment
├── Ophthalmoscopy (disc evaluation)
└── Ideally: pachymetry + gonioscopy for high-risk individuals

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QUICK EXAM REVISION TABLE

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Source: Kanski's Clinical Ophthalmology: A Systematic Approach, 10th Edition — Chapter 11: Glaucoma